The long-term function of this research program is to relate visual deficits to the underlying cellular pathophysiology of disease processes, with the current focus exclusively on glaucoma. The proposed research applies a quantitative cortical neural pooling model to analysis of perimetric damage produced by glaucoma, with the goals of reducing perimetric variability and improving relations between clinical measures of glaucomatous damage. There are three Specific Aims:
Specific Aim 1) To optimize contrast sensitivity perimetry (CSP) for clinical use in patients with glaucoma, using a quantitative neural model for perimetry. Our neural model will be used to optimize CSP parameters and algorithms in terms of four factors: screening (identify defects), test-retest (identify progression), characterization (identify pattern of damage), and relations with structural measures.
Specific Aim 2) To analyze relations between conventional automated perimetry (CAP) and imaging measures in data from the United Kingdom Glaucoma Treatment Study (UKGTS), using a quantitative neural model. A large prospective longitudinal dataset will be analyzed in terms of model predictions relating perimetric sensitivity with results from four different imaging tests.
Specific Aim 3) To assess long-term fluctuation versus progression within and between perimetric and structural measures of glaucomatous damage, using a quantitative neural model for perimetry. A prospective longitudinal study will be conducted to test predictions of the model concerning relations between CSP and standard clinical measures, both perimetric and imaging.
Perimetry measures visual function across the visual field, and is used routinely for diagnosing and following patients with glaucoma, one of the leading causes of blindness in the US and globally. The proposed research will produce a deeper scientific understanding of perimetry, and will lead to improved methods for using perimetry in clinical studies, treatment trials and care of individual patients. The potential public health benefit is substantial, given the large number of patients with glaucoma.
| Alluwimi, Muhammed S; Swanson, William H; King, Brett J (2018) Identifying Glaucomatous Damage to the Macula. Optom Vis Sci 95:96-105 |
| Ramezani, Koosha; Marín-Franch, Iván; Hu, Rongrong et al. (2018) Prediction Accuracy of the Dynamic Structure-Function Model for Glaucoma Progression Using Contrast Sensitivity Perimetry and Confocal Scanning Laser Ophthalmoscopy. J Glaucoma 27:785-793 |
| Swanson, William H; Dul, Mitchell W; Horner, Douglas G et al. (2017) Individual differences in the shape of the nasal visual field. Vision Res 141:23-29 |
| Price, Derek A; Swanson, William H; Horner, Douglas G (2017) Using perimetric data to estimate ganglion cell loss for detecting progression of glaucoma: a comparison of models. Ophthalmic Physiol Opt 37:409-419 |
| Gardiner, Stuart K; Swanson, William H; Demirel, Shaban (2016) The Effect of Limiting the Range of Perimetric Sensitivities on Pointwise Assessment of Visual Field Progression in Glaucoma. Invest Ophthalmol Vis Sci 57:288-94 |
| Ashimatey, Bright S; Swanson, William H (2016) Between-Subject Variability in Healthy Eyes as a Primary Source of Structural-Functional Discordance in Patients With Glaucoma. Invest Ophthalmol Vis Sci 57:502-7 |
| Swanson, William H; Dul, Mitchell W; Horner, Douglas G et al. (2016) Contrast sensitivity perimetry data from adults free of eye disease. Data Brief 8:654-8 |
| Dul, Mitchell; Ennis, Robert; Radner, Shira et al. (2015) Retinal adaptation abnormalities in primary open-angle glaucoma. Invest Ophthalmol Vis Sci 56:1329-34 |
| Swanson, William H; Horner, Douglas G (2015) Assessing assumptions of a combined structure-function index. Ophthalmic Physiol Opt 35:186-93 |
| Huang, Gang; Luo, Ting; Gast, Thomas J et al. (2015) Imaging Glaucomatous Damage Across the Temporal Raphe. Invest Ophthalmol Vis Sci 56:3496-504 |
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